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BMJ Case Rep. 2010; 2010: bcr09.2009.2308.
Published online Mar 30, 2010. doi:  10.1136/bcr.09.2009.2308
PMCID: PMC3029149
Findings that shed new light on the possible pathogenesis of a disease or an adverse effect
Perforation of Meckel’s diverticulum secondary to a large faecolith
Henry Ferguson, Soni Soumian, and Jan Dmitrewski
Department of General Surgery, Russells Hall Hospital, Pensnett Road, Dudley DY1 2HQ, UK
Correspondence to Henry Ferguson, fergusonh/at/doctors.org.uk
A 79-year-old woman presented with a 4 day history of central abdominal pain and vomiting. Clinical examination revealed a distended abdomen with predominantly right sided tenderness. Following an initial period of supportive treatment pending further imaging, evolving abdominal signs became evident. Based on the suspicion of a perforated hollow viscus, an emergency laparotomy was carried out. Operative findings were of a Meckel’s diverticulum with evidence of pressure necrosis and perforation near its apex, which was distended due to a 6 cm faecolith. Resection and primary anastomosis was performed. Despite a lower respiratory tract infection, the patient was deemed clinically stable enough to be discharged on the 24th postoperative day.
Background
While Meckel’s diverticulum is relatively common, with an incidence estimated at between 2–3%,1 complications are infrequent and most commonly occur in the first 20 years of life. A search of Medline and Embase revealed only around 40 case reports of perforated Meckel’s diverticulitis reported in the literature in the last 30 years. Perforation of this kind is rarely seen within an elderly patient demographic, and perforation as a result of presumed pressure necrosis from a faecolith has only been described once before.2
A 79-year-old woman presented to the accident and emergency department with a 4 day history of increasing ‘gripping’ pain in the central abdomen, associated with copious vomiting, and bouts of diarrhoea. This was associated with a lack of appetite, but her presentation was otherwise relatively non-specific. Her only past medical history was of asthma requiring regular bronchodilators but no steroids. She had no previous abdominal operations.
She was a lifelong non-smoker, and took only minimal alcohol. She had no relevant family history.
On examination, she was pyrexial (38.1°C), tachycardic (130 beats/min, regular rhythm), and normotensive (127/70 mm Hg). Her abdomen was distended and generally tender, predominantly in the right upper and lower quadrants. While her abdomen was tympanic to percussion, it was not rigid, and did not exhibit any firm signs of peritonism. Her bowel sounds were noted to be present, and high pitched. Rectal examination revealed only soft stool.
Investigations
Full blood count was normal with a white cell count of 4.7×109/l. Serum biochemistry indicated acute renal impairment (urea 19.4 mmol/l, creatinine 166 mmol/l), but no other abnormalities.
Erect chest radiograph did not indicate free peritoneal gas, while a supine abdominal radiograph showed a centrally placed, moderately dilated small bowel loop (fig 1), but firmly diagnostic features were lacking.
Figure 1
Figure 1
Plain abdominal radiograph on admission showing a few non-diagnostic small bowel loops.
Differential diagnosis
The working diagnosis on admission was that of small bowel obstruction, with a view to further diagnostic imaging with concurrent fluid resuscitation, before surgical exploration via laparotomy.
During this period of fluid resuscitation, serial abdominal examination yielded developing signs of generalised peritonitis, and subsequently pronounced rigidity and percussion tenderness were identified. Consideration was given at this time to an expeditious computed tomography (CT) scan, but in discussion with radiological and anaesthetic colleagues it was felt that it would not significantly alter management. The decision was therefore made to proceed to immediate laparotomy.
Operative findings were of 500 ml of free purulent fluid upon entering the peritoneal cavity; following systematic examination of the viscera, a firm, inflamed ileal diverticulum was identified 75 cm proximal to the ileocaecal valve (fig 2), which showed a focal perforation at its apex. Wedge resection of this perforated ileal segment followed by primary anastomosis was performed. Inspection of the excised specimen showed a distended diverticulum with a 6 cm faecolith within its lumen (fig 3). Histology confirmed the findings of a focal area of necrosis within an ileal diverticulum, with localised perforation. There was no evidence of ectopic mucosa, or direct vascular occlusion, and it was concluded that pressure necrosis was the most likely cause of perforation.
Figure 2
Figure 2
Intraoperative image showing the enlarged and distended Meckel’s diverticulum with evidence of perforation.
Figure 3
Figure 3
A 6 cm faecolith found within the perforated Meckel’s diverticulum.
Outcome and follow-up
Postoperatively, the patient was transferred to the surgical high dependency unit for standard postoperative care, and continued on a course of intravenous antibiotics (amoxicillin 1 g three times daily, gentamicin 320 mg once daily, metronidazole 500 mg three times daily) for a further 3 days.
The patient’s postoperative recovery was complicated by a lower respiratory tract infection, but she was deemed clinically stable enough to be discharged home on the 24th postoperative day.
Meckel’s diverticulum is the most common congenital abnormality in the small bowel. It is estimated to occur in 2–3% of the population.1 Of these, approximately one in five are thought to be symptomatic.3 A complication sufficient to cause an acute surgical admission is estimated to occur in 4.3% of children, falling to 3% of adults, and approaching 0% in the elderly.4 The most common clinical manifestations in descending order of frequency are haemorrhage, inflammation, bowel obstruction, intussusception, umbilical fistula and tumour.5
Perforation is noted to be an occasional consequence of acute Meckel’s diverticulitis, but the exact rate of this has not been reported. The aetiology of perforation is commonly attributed to ectopic gastric mucosa,5 or a narrow diverticulum neck width leading to a process analogous to that involved in acute appendicitis.6
A review of the literature has yielded only one previous incidence of a faecolith causing a perforated Meckel’s diverticulum.2 In this case, a 56-year-old patient underwent laparotomy, and operative findings were of a perforated Meckel’s diverticulum, with a faecolith found in the pelvis. This is the first case reported in an elderly patient, and also the first case encountered with the faecolith in situ, with photographic evidence.
Learning points
  • Perforation of Meckel’s diverticulum due to a luminal faecolith can and does occur.
  • Perforated Meckel’s diverticulitis is an uncommon cause of generalised peritonitis, but remains a diagnostic possibility, even in patients in their late 70s.
  • Early intervention without preoperative imaging is often necessary when a patient deteriorates—it always pays to keep an open mind as to what you may find.
Footnotes
Competing interests: None.
Patient consent: Patient/guardian consent was obtained for publication.
1. Cullen JJ, Kelly KA, Moir CR, et al. Surgical management of Meckel’s diverticulum. An epidemiologic, population-based study. Ann Surg 1994; 220: 564–9. [PubMed]
2. Loh, D Perforated Meckel’s diverticulum caused by faecolith. ANZ J Surg June 2008; 78: 518–19. [PubMed]
3. Mackey WC, Dineen PA. A fifty year experience with Meckel’s diverticulum. Surg Gynecol Obstet 1983; 156: 56–64. [PubMed]
4. Soltero MJ, Bill AH. The natural history of Meckel’s diverticulum and its relation to incidental removal. Am J Surg 1976; 132: 168–73. [PubMed]
5. Willam R. Management of Meckel’s diverticulum. Br J Surg 1981; 68: 477–80. [PubMed]
6. Malhotra S. Gangrene of Meckel’s diverticulum secondary to axial torsion. Am J Gastroenterol 1998; 93: 1373–5. [PubMed]
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